Vascular calcification: Not so crystal clear

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Vascular calcification: Not so crystal clear W.C. O'Neill Kidney International Volume 71, Issue 4, Pages 282-283 (February 2007) DOI: 10.1038/sj.ki.5002119 Copyright © 2007 International Society of Nephrology Terms and Conditions

Figure 1 Formation of apatite is at least a two-step process that begins with formation of amorphous calcium phosphate followed by spontaneous conversion to apatite. The first reaction does not occur at normal plasma concentrations, which are below the solubility product for CaHPO4. The second reaction is essentially irreversible at physiologic pH and is normally inhibited in vivo. Thus, ectopic calcification requires factors that favor the first reaction and abrogate inhibition of the second reaction. Kidney International 2007 71, 282-283DOI: (10.1038/sj.ki.5002119) Copyright © 2007 International Society of Nephrology Terms and Conditions

Figure 2 Potential mechanisms for vascular calcification in renal failure. Pyrophosphate (PPi) and Matrix Gla protein (MGP) are key inhibitors of apatite formation. PPi may be deficient in uremic vessels by virtue of hydrolysis to orthophosphate (Pi) increased alkaline phosphatase (Alk phos) activity. Decreased carboxylation of MGP could contribute to apatite formation, but whether this occurs in uremia is unknown. Alkalemia at levels that occur after hemodialysis favors both reactions and increases calcification of vessels in vitro. Lastly, Mg2+ stabilizes amorphous calcium phosphate and can drive formation of whitlockite. Kidney International 2007 71, 282-283DOI: (10.1038/sj.ki.5002119) Copyright © 2007 International Society of Nephrology Terms and Conditions